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Ginger provides neuroprotection in experimental model of traumatic brain injury
Author(s) -
Sahin Kazim,
Kilic Ertugrul,
Balcikanli Zeynep,
Ates Nilay,
Orhan Cemal,
Tuzcu Mehmet,
Juturu Vijaya
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.795.16
Subject(s) - neuroprotection , traumatic brain injury , glial fibrillary acidic protein , neurotrophic factors , pharmacology , inflammation , medicine , antioxidant , chemistry , biochemistry , immunohistochemistry , receptor , psychiatry
Ginger (Zingiberaceae family) containing gingerols, shogaols, zingerone and volatile oils active compounds, exerts anti‐inflammatory, antioxidant, antiplatelet, fat loss, prevention of cardiovascular disease and anticancer activity. In spite of these known effects, the underlying mechanisms in the signaling pathways that ginger protects the brain after brain trauma are largely unknown. Therefore, the objective of this study was to examine the administration of ginger extract (Gingever®) to improve histopathological results and to demonstrate neuroprotective activity with antioxidative and anti‐inflammatory properties following TBI. Brain injury was induced using a cold trauma model in male mice that were treated with ginger extract (50 mg/kg) or vehicle via intraperitoneal administration just after TBI. Mice were divided into two groups: TBI+vehicle group and TBI+ ginger extract group. Our results show that ginger administration decreased infarct volume by decreasing nuclear factor‐κB (NF‐κB), interleukin 1‐beta (IL‐1b), and glial fibrillary acidic protein (GFAP) and by increasing neurotrophic factor BDNF, growth‐associated protein‐43 (GAP‐43), neural cell adhesion molecule (ICAM) and nuclear factor erythroid 2‐related factor 2 (Nrf2) in the brain. Our findings suggested that ginger promotes neuroprotection following TBI by inhibiting the levels of inflammation, NFkB, and GFAP, and increasing GAP‐43 and Nrf2 levels. Support or Funding Information This research was funded by the OmniActive Health Technologies Inc, NJ, USA and partly supported by the Turkish Academy of Sciences (Ankara, Turkey, KS). This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .